A. Field of the Invention
This invention relates to methods and devices for analysis of the electrical activity of the heart (Electrocardiography) and more particularly to the field known as High Resolution Electrocardiography, which is concerned with detecting abnormalities not apparent on conventional electrocardiograms. The specific and major purpose intended for the present invention is the clinical evaluation of medical patients for risk of life-threatening arrhythmias of the heart. However, both the method and apparatus are potentially suitable for research into and diagnosis of a wide variety of other disorders of cardiac electrical activity, and the analysis of other bio-electrical signals such as those recorded on an Electroencephalogram (EEG).
B. Description of the Background Art
In order to fully comprehend the purpose and method of the present invention, it is necessary to be familiar with certain standard physiological and electrocardiographic (ECG) nomenclature. Relevant portions of that nomenclature are briefly summarized here, for the benefit of the reader not conversant with medical terminology.
The pumping action of the normal heart results from the orderly contraction of millions of individual muscle cells. Each heart beat is initiated by the spontaneous periodic activity of certain specialized cells of a structure known as the sino-atrial node. Activation of heart muscle cells is initiated by an electrical pacing signal generated in the sino-atrial node and propagated by specialized tissues known collectively as "the conducting system" of the heart. At the cellular level, the process of activation is known as "depolarization" since it involves transient changes in the electrical potential across the cell membrane mediated by the passage of ions The process of recovery to the normal "resting" state is referred to as "repolarization."
The spread of the wavefront of electrical depolarization through the atria (or "primer pumping chambers") of the heart gives rise to the deflection on the electrocardiogram known as the "P" wave. Contraction of the main cardiac pumping chambers, or ventricles, is associated with a biphasic or multiphasic deflection of the ECG waveform known as the "QRS complex." Spread of the wavefront of electrical recovery (repolarization) through the ventricles gives rise to the "T" wave of the ECG. The time interval between the end of the QRS complex and the T Wave, referred to as the "ST segment" is normally free from electrical activity, but may harbor small amplitude signals known as "late potentials" which extend out beyond the end of the QRS complex (viewed at ordinary magnification) into the ST segment. All of the components of ECG waveforms result from the synchronous spread of electrical signals associated with the activation or recovery of individual cardiac cells, across millions of such cells.
Over 50,000 people die annually in the USA of unexpected or sudden cardiac death, almost always from a catastrophic failure of normal electrical conduction within the heart known as ventricular fibrillation. Instead of the normal orderly and synchronous contraction of the heart muscle cells necessary for pumping of blood to occur, individual muscle fibers contract in a random and totally disorganized fashion This arrhythmia (abnormal cardiac rhythm) frequently occurs in association with a myocardial infarction ("heart attack") either within the first minutes, hours, or sometimes months to years later, but is also the final common pathway for almost all forms of death from cardiac causes. Ventricular fibrillation is a terminal event because no blood at all is pumped and vital organs such as the brain die from lack of oxygen within minutes unless either the rhythm is corrected ("defibrillation") or the circulation is artificially supported by some other means such as CPR or cardio-pulmonary bypass ("heart-lung machine").
A frequent immediate predecessor to ventricular fibrillation is another arrhythmia known as ventricular tachycardia ("VT") during which, although some blood is pumped, the heart rate is usually much more rapid than the maximum rate at which the heart may function effectively as an efficient pump. This excessive heart rate frequently results in symptoms such as loss of consciousness or lightheadedness. VT may spontaneously revert to a more normal heart rhythm ("non-sustained") or be prolonged for more than 30 seconds ("sustained"), in which latter case the development of symptoms or progression to ventricular fibrillation is much more common.
Despite the existence of a wide variety of more or less successful treatments such as drug therapy, surgery or implantable defibrillators for the prevention or correction of ventricular arrhythmias, their use is not without risk or expense of its own. Classical electrocardiography as practiced for several decades is unfortunately very poor at predicting who is likely to suffer such an event. Although it is known that increased risk is associated with certain states such as a severely damaged or dilated left ventricle (main pumping chamber of the heart), there remains an urgent need for a means of delineating those patients at significant risk, who might truly benefit from aggressive therapies, from amongst the vast majority of potential candidates in whom the risk of life threatening arrhythmia is low and for whom aggressive (or expensive) therapies may actually do more harm than good. Such an arrhythmia risk screening test should preferably be "non-invasive," i.e., not require breaking of the skin surface and free from risk and discomfort to the patient.
The most reliable method currently available for predicting likelihood of development of a lethal arrhythmia is a diagnostic procedure called "electrophysiological study" (EP) during which slender wires ("pacing catheters") are introduced through the skin into a large vein and advanced under X-ray guidance into the heart chambers themselves. Using a device attached to the wires, which generates electrical impulses similar to those produced by a pacemaker, the interior surface of the heart is subjected to electrical stimulation pulses in an attempt to induce VT. If it proves possible to induce ventricular tachycardia which is " (of one shape or type) and "sustained" (not spontaneously terminating) the patient is deemed to be much more likely to spontaneously develop a lethal rhythm disorder. Unfortunately, EP study is invasive, requires admitting the patient to a hospital, is often distressing to the patient who may need to be defibrillated out of a successfully induced arrhythmia, and is time, labor and cost intensive.
Among available non-invasive arrhythmia risk assessment techniques, so-called "late potential analysis" has received most attention both in the literature and commercially. The patents of Simson, U.S. Pat. No. 4,422,459, Dec. 27, 1983, Netravali, U.S. Pat No. 4,458,691, Jul. 10, 1984, and Strick, U.S. Pat. No. 4,492,235, Jan. 8, 1985, teach a method currently in widespread use on real-time ECGs. Many variants of the method have been advocated in the medical literature. Late potentials are signals of very low amplitude (less than 40 uV versus about 1 mV for the main ECG signal proper) and thus require employment of a special noise reduction technique known as "signal averaging" for them to be discernible above the background noise. Their presence beyond the end of the normal QRS complex is about 70-80% predictive for inducibility of sustained monomorphic VT at EP study and hence development of a serious spontaneous ventricular arrhythmia. However, late potential analysis cannot be used at all in the presence of certain relatively common types of ECG abnormality, and its specificity and sensitivity leave much to be desired.
The method of Simson teaches identification of late potentials by analysis in the time domain only, without any attempt to explicitly analyze their frequency, or spectral content. Bipolar ECG signals from three orthogonal surface leads are bidirectionally filtered and then algebraically summed into a single "vector magnitude" upon which certain characteristics of the terminal QRS signal are then measured. Late potentials are deemed to be present or absent depending upon the duration and amplitude of the terminal QRS region. As already noted, late potentials are not infrequently found (by time domain techniques) in perfectly normal, healthy individuals. The present invention teaches among other things, a novel method of distinguishing such "false positive" late potentials from those associated with serious arrhythmia risk, based upon frequency spectra, or their "spectrocardiographic" features.
In U.S. Pat. No. 4,680,708, Jul. 14, 1987, Ambos, Cain & Sobel claim a frequency domain technique for late potential identification using Fourier analysis of a single, relatively long segment of ECG signal positioned over the terminal QRS region. Abnormality is allegedly characterized by presence of secondary high frequency peaks and an excess ratio of high frequencies to low frequencies.
In U.S. Pat. No. 4,883,065, one of the present inventors, Kelen, disclosed a novel system for the analysis of late potentials from long-term recordings of ECGs made on an ambulatory monitor, e.g., a Holter monitor.
The present invention teaches spectral mapping of multiple overlapping ECG signal segments, spanning the whole QRS complex, with abnormality recognizable by visual features of three dimensional maps and computed parameters not disclosed or suggested by Cain or any other prior art known by the present inventors. The novel method and apparatus of diagnosis via spectral feature analysis used in the present invention is applicable to the analysis of ECG signals recorded on Holter monitor tapes, as well as in real time.